1173
cobalamin deficiency.2 Untreated cobalamin deficiency progresses subacute combined system disease with degenerative changes of the dorsal and lateral columns,3 and in severe cases some affected areas of the spinal cord are grossly atrophic.4 to
MRI has proved to be an important step in the evaluation of the central nervous system. A recent MRI study on demyelination of the central nervous system in children with inborn errors of the methyl-transfer pathway revealed a bright signal that resolved on correction of the metabolic deficiencies. These metabolic deficiencies cause a demyelinating process similar to that associated with cobalamin deficiency. The MRI picture in multiple sclerosis also resembles that seen in our patient. However, these changes are not seen in the spinal cord without concomitant brain abnonnalities6 and they would not be expected to change with cobalamin administration, as they did in our patient. Department of Medicine, Brown University School of Medicine, Miriam Hospital, Providence, Rhode Island 02906, USA
J. P. TRACEY FRED J. SCHIFFMAN
1. Beck WS. Neuropsychiatric consequences of cobalamin deficiency. In. Stollerman GH, ed. Curr Conc Intern Med 1991; 36: 38-41 2. Healton EB, Savage DG, Brust JC, et al. Neurologic aspects of cobalamin deficiency. Medicine 1991; 70: 229-45. 3. Adams JH, Corsellis J, Duchey L. In: Greenfield’s neuropathology, 4th ed. New York: Wiley, 1984: 588 4. Moms JH, Schoene WC. The nervous system. In: Robbins SL, ed. Pathologic basis of disease, 3rd ed. Philadelphia: Saunders, 1984: 1421. 5. Surtees R, Leonard J, Austin S. Association of demyelination with deficiency of cerebrospinal-fluid S-adenosylmethionine in inborn errors of methyl-transfer pathway. Lancet 1991; 338: 1550-54. 6. Modic MT. MRI of the spine. Radiol Clin N Am 1986; 24: 242.
Grass pollen and asthma SiR,-Cenk Suphioglu and colleagues (March 7, p 569) present data that support suspicions that pollen grains are too large to penetrate lower airways. What they have shown, and have shown well, is that pollen starch granules can precipitate episodes of airway narrowing. However, the conclusions drawn are not warranted since recognised criteria for causation are not satisfied. There is no evidence that particles or pollen allergy cause the disease asthma. Suphioglu et al have not shown any association with the incidence of asthma because this was not measured; this misleading use of words may encourage people to believe that avoidance of pollen starch can prevent the disease. Our data from children in New South Wales show that although many asthmatics are allergic to ryegrass, which is clearly associated with symptoms, it is a much less important risk factor for "current asthma" than allergy to housedust mites, alternaria, or cat dander. Until avoidance of all of these allergens is undertaken, it is extremely unlikely that avoidance of ryegrass allergen will have any impact on the prevalence of asthma. Nor do we yet know if allergen avoidance can prevent asthma from
developing. Department of Medicine, University of Sydney,
ANN J. WOOLCOCK
Sydney, NSW 2006, Australia
SiR,-Suphioglu and colleagues suggest a mechanism by which starch granules released from ryegrass pollen grains after rainfall elicit allergic asthma-namely, that the granules are small enough to enter the lower airways. We report our experience in 207 patients with allergic rhinitis due to Parietaria judaica pollen, 193 with rhinitis due to Dermatophagoides pteronyssinus, and 31 healthy controls. Our aim was to establish the presence and the severity of allergic conjunctivitis. The study was done during the pollen season
(spring, 1991). Clinical evaluations were done on a four-point rating scale (0 = no symptom, 1 = mild, 2 moderate, 3 severe) and the cytological findings were scored (0-4, no cells or 1-5, 6-19,11-30, or > 30 cells per microscope field). 2 weeks before the study (run-in period) allergic individuals recorded symptoms of conjunctivitis every day =
=
diary card (itching, photophobia, lacrimation, foreign-body sensation).2 No antiallergic drugs were allowed during the run-in. Conjunctival symptoms were more common in the pollensensitive patients than in the house-dust-mite-sensitive patients on a
.,.y..
B
E3
-
y
y ...........
Par jsensitive Dp sensitive subjects
Symptom scores on patients’ diary cards and sign scores and total cellular (cytology) scores reported by physicians. Par j = Pjudaica; Dp D pteronyssinus. =
(89% [185/207] vs 34% [67/193]). Furthermore, their clinical and
cytology scores were greater (figure). The controls showed neither clinical nor cytological reactions. All conjunctival scrapings of pollen-sensitive patients showed not only an inflammatory infiltrate (mainly neutrophils and eosinophils) but also several pollen grains (7-8 per field at 250 x focus); pollen granules frequently seemed to be ruptured along the outer envelope, thus releasing cytoplasmic contents. The greater severity of findings in pollen-sensitive subjects could be related to these granules in the conjunctiva. No pollen granules were found in conjunctival scrapings from the other patient group or from the controls. P judaica pollen grains are subspheroidal and are rapidly ruputed by osmotic shock (ie, contact with wet surfaces), releasing allergic contents through the germinal pore.2 Our findings fit very well with those of Suphioglu and colleagues. All these data suggest a combined mechanism whereby the conjunctiva of pollen-sensitive individuals selectively captures P judaica grains that trigger a specific-IgE-mediated response with inflammatory reaction, including the cellular infiltrate and mediator release.3 Moreover, histamine produces capillary leakage with albumin transudation, which could retain pollen grains, so prolonging allergen persistence and setting up a vicious circle with a clinically more severe pattern. A similar sequence could be hypothesised in pollen-associated asthma. Allergy and Clinical Immunology Service, Department of Internal Medicine and Eye Clinic, University of Genoa, 16132 Genoa, Italy, and Pathology Department, Alessandria Hospital
G. CIPRANDI S. BUSCAGLIA P. M. CERQUETI M. COSIMI G. W. CANONICA
Ciprandi G, Buscaglia S, Pesce GP, Marchesi E, Canonica GW. Protective effect of loratadine on conjunctival provocation test. Int Arch Allergy Clin Immunol (in press). 2. Solomon WM, Mathews KP. Aerobiology and inhalant allergens. In: Middleton E Jr, Reed CE, Ellis EF, Adkinson JF Jr, Yunginger JW, eds. Allergy: principles and practice, 3rd ed. St Louis: Mosby, 1988: 312. 3. Proud D, Sweet J, Stein P, et al. Inflammatory mediator release in conjunctival provocation of allergic subjects with allergen. J Allergy Clin Immunol 1990; 85: 1.
896-905.
Chlamydia pneumoniae infection and asthma SIR,-Dr Crane and colleagues (March 28, p 814) speculate that worldwide increases in asthma morbidity, mortality, and prevalence could be attributable to diagnostic transfer, changes in the delivery of health care, or increased diagnosis or self-reporting. I recent
would add another possible explanation that has not received the attention it deserves-increasing worldwide prevalence of Chlamydia pneumoniae infection. Preliminary epidemiological and clinical data support the suggestion that C pneumoniae infection may play a part in this increase in asthma. C pneunwniae infection has been associated with wheezing, asthmatic bronchitis, and adult-onset asthma in a clinical population.2 A patient from this study in whom asthma began in association with serologically confirmed acute C pneumoniae infection had a complete remission of symptoms after lengthy anti-chlamydial therapy. After a symptom-free interval of two
1174
years, this patient had renewed chronic wheezing in association with a serologically documented reinfection with C pneumoniae. In Finland, increasing prevalence of C pneumoniae infection since the 1970s3 correlates with striking increases in adult asthma 4 Since
C TRACHOMATIS IN FAMILIES OF SEVEN POSITIVE "ASTHMATIC" CHILDREN (A-G)
C pneumoniae is a recognised cause of bronchitis, we should also increase in acute bronchitis in adults that correlates with a rise in adult asthma between 1970 and 1981 in England and Wales.s There is also a temporal relation between the appearance of C pneumoniae infection6 and adult asthmain Denmark. I agree with Crane et al that appropriate use of bronchodilator medication is important to keep to a minimum the adverse effects on asthma. I would urge asthma researchers also to consider the possibility that C pneumoniae infection could be one of the underlying (and potentially treatable) causes of a disease whose management has so far been only palliative.
note an
Arcand Park Clinic, 3434 East Washington Ave, Madison WI 53704, USA
DAVID L. HAHN
1. Bone RC.
Chlamydial pneumonia and asthma: a potentially important relationship. JAMA 1991; 266: 265. 2. Hahn DL, Dodge R, Golubjatnikov R. Association of Chlamydia pneumomae (strain TWAR) infection with wheezing, asthmatic bronchitis and adult-onset asthma. JAMA 1991; 266: 225-30. 3. Puolakkainen M, Ukkonen P, Saikku P. The seroepidemiology of Chlamydiae in Finland over the period 1971 to 1987. Epidem Infect 1989; 102: 287-95. 4. Klaukka T, Peura S, Martikainen J. Why has the utilization of antiasthmatics increased in Finland? J Clin Epidermiol 1991; 44: 859-63. 5. Fleming DM, Crombie DL. Prevalence of asthma and hayfever in England and Wales. Br Med J 1987; 294: 279-83. 6. Grayston JT. TWAR. A newly discovered Chlamydia organism that causes acute respiratory tract infections. Infect Med 1988; 5: 215-48. 7. Pedersen P, Weeke ER. Epidemiology of asthma in Denmark. Chest 1987; 91: 107-14S.
Chlamydia trachomatis infection in children with wheezing simulating asthma SIR,-Ghlamydia trachomatis, according to WHO estimates is, after Trichomonas vaginalis, the most frequent sexually acquired pathogen in adults, carrying the possibility of contamination at birth of babies bom to infected mothers. It is difficult to establish how older children become infected with this organism, sexual abuse apart, but serological evidence of C trachomatis is found in an increasing proportion of the population with time. The rate varies not just with age but also with socioeconomic and environmental factors; in prepubertal age groups, rates of 26-7% and 47 2% have been reported.1,2 We have looked for C trachomatis infection in 20 wheezing children (13 boys, 7 girls; aged 6 months to 10 years, mean 32 months). They were negative on allergic evaluation and did not respond to bronchodilator agents. Pharyngeal and conjunctival swabs, for culture on McCoy cells and for a direct immunofluorescent test with monoclonal antibodies, were collected. In an attempt to trace the route of transmission we also examined the families of positive children. C trachomatis was identified by culture in 7 (35%) children in the pharynx, with concordance of results by both methods in only 1 case. In these 7 children, the organism was identified in the conjunctiva in 6; 4 of these had eye symptoms, present at the time of examination in 2. Treatment with erythromycin ethylsuccinate (50 mg/kg daily) for 2 weeks was successful in 6 of the 7 cases. In the other child, a further course of the same antibiotic eradicated the infection. C trachomatis was demonstrated by culture of at least one site in several parents of positive children (table). In one family, where the parents were both negative, we found on further inquiry that other relatives living in the same apartment were positive. Doxycycline 200 mg twice a day for 21 days was given to the adult relatives and the cousin was treated with erythromycin for 2 weeks. Control swabs after completion of this therapy were all negative. The asthmatic symptoms remitted in all 7 C trachomatis infected children, and the ocular symptoms also stopped. At 1-year follow-up these 7 children remained negative for C trachomatis on culture and had had no further asthma attacks. C pneumoniae strain TWAR can be excluded as the explanation in these 7 wheezing children because this agent grows only on HeLa
*Results for culture, immunofluorescence t- irrelevant or not done
(direct)
=
229 cells and
not on
the
McCoy
cells
we
used for
our
isolation
procedures. In these
children, C trachomatis infection could have arisen
through family contacts, the trigger being a primary infection in one adult.3 The findings in the family living in an overcrowded apartment suggest the possibility of C trachomatis spreading to children from adults directly by close daily contact with secretions (eg, saliva, tears) and/or hands or indirectly through fomites, toys, towels, and bedlinen, for example. Our data indicate that wheezing may be another clinical expression of C trachoma tis infection and that this organism should be sought as a routine in children who wheeze but have no demonstrable allergy and do not respond to the usual anti-asthmatic medications.
Supported by grant 9103613 from CNR P.F. FATMA. Institute of Paediatrics, La Sapienza University, and CNR Institute of Experimental Medicine, 00161 Rome, Italy
MARIA BAVASTRELLI MARIO MIDULLA DANIELA ROSSI MARCO SALZANO
1. Black SB, Grossman M, Cles L, Schachter J. Serologic evidence of infection in children. Pediatr 1981; 98: 65-67. J 2. San Joaquin VH, Rettig PJ, Newton JY, Marks MI. Prevalence of antibodies in children. Am J Dis Child 1982; 136: 425-27. 3. Medici A, Sollecito D, Rossi D, Midulla M. Family outbreak of trachomatis. Lancet 1988; ii: 682.
chlamydial chlamydial
Chlamydia
Reversal by ceftriaxone of dilated cardiomyopathy Borrelia burgdorferi infection SIR,-Dilated cardiomyopathy is a life-threatening disorder, which, when progressive, leads to chronic heart failure. It has been suggested that, in several cases, Borrelia burgdorferi could be associated with chronic myocarditis and dilated cardiomyopathy. Thus B
burgdorferi could be isolated and cultured from a myocardial biopsy specimen in a patient with dilated cardiomyopathy.1 However, data about B burgdorferi in dilated cardiomyopathy and its treatment are scant, especially with respect to reversibility of changes in myocardial functions We report a prospective study in which we examined specifically for B burgdorferi infection, serum for IgG and IgM (ELISA), and the history in 42 patients with dilated cardiomyopathy (mean left-ventricular ejection fraction [LVEF] 30% [SEM 12%] assessed by cardiac catheterisation). 9 (21 %) patients with a mean LVEF of 34% (2-2%) were seropositive for B burgdorferi, and 7 of those had a typical history of tick bite and erythema chronicum
cobalamin deficiency.2 Untreated cobalamin deficiency progresses subacute combined system disease with degenerative changes of the dorsal and lateral columns,3 and in severe cases some affected areas of the spinal cord are grossly atrophic.4 to
MRI has proved to be an important step in the evaluation of the central nervous system. A recent MRI study on demyelination of the central nervous system in children with inborn errors of the methyl-transfer pathway revealed a bright signal that resolved on correction of the metabolic deficiencies. These metabolic deficiencies cause a demyelinating process similar to that associated with cobalamin deficiency. The MRI picture in multiple sclerosis also resembles that seen in our patient. However, these changes are not seen in the spinal cord without concomitant brain abnonnalities6 and they would not be expected to change with cobalamin administration, as they did in our patient. Department of Medicine, Brown University School of Medicine, Miriam Hospital, Providence, Rhode Island 02906, USA
J. P. TRACEY FRED J. SCHIFFMAN
1. Beck WS. Neuropsychiatric consequences of cobalamin deficiency. In. Stollerman GH, ed. Curr Conc Intern Med 1991; 36: 38-41 2. Healton EB, Savage DG, Brust JC, et al. Neurologic aspects of cobalamin deficiency. Medicine 1991; 70: 229-45. 3. Adams JH, Corsellis J, Duchey L. In: Greenfield’s neuropathology, 4th ed. New York: Wiley, 1984: 588 4. Moms JH, Schoene WC. The nervous system. In: Robbins SL, ed. Pathologic basis of disease, 3rd ed. Philadelphia: Saunders, 1984: 1421. 5. Surtees R, Leonard J, Austin S. Association of demyelination with deficiency of cerebrospinal-fluid S-adenosylmethionine in inborn errors of methyl-transfer pathway. Lancet 1991; 338: 1550-54. 6. Modic MT. MRI of the spine. Radiol Clin N Am 1986; 24: 242.
Grass pollen and asthma SiR,-Cenk Suphioglu and colleagues (March 7, p 569) present data that support suspicions that pollen grains are too large to penetrate lower airways. What they have shown, and have shown well, is that pollen starch granules can precipitate episodes of airway narrowing. However, the conclusions drawn are not warranted since recognised criteria for causation are not satisfied. There is no evidence that particles or pollen allergy cause the disease asthma. Suphioglu et al have not shown any association with the incidence of asthma because this was not measured; this misleading use of words may encourage people to believe that avoidance of pollen starch can prevent the disease. Our data from children in New South Wales show that although many asthmatics are allergic to ryegrass, which is clearly associated with symptoms, it is a much less important risk factor for "current asthma" than allergy to housedust mites, alternaria, or cat dander. Until avoidance of all of these allergens is undertaken, it is extremely unlikely that avoidance of ryegrass allergen will have any impact on the prevalence of asthma. Nor do we yet know if allergen avoidance can prevent asthma from
developing. Department of Medicine, University of Sydney,
ANN J. WOOLCOCK
Sydney, NSW 2006, Australia
SiR,-Suphioglu and colleagues suggest a mechanism by which starch granules released from ryegrass pollen grains after rainfall elicit allergic asthma-namely, that the granules are small enough to enter the lower airways. We report our experience in 207 patients with allergic rhinitis due to Parietaria judaica pollen, 193 with rhinitis due to Dermatophagoides pteronyssinus, and 31 healthy controls. Our aim was to establish the presence and the severity of allergic conjunctivitis. The study was done during the pollen season
(spring, 1991). Clinical evaluations were done on a four-point rating scale (0 = no symptom, 1 = mild, 2 moderate, 3 severe) and the cytological findings were scored (0-4, no cells or 1-5, 6-19,11-30, or > 30 cells per microscope field). 2 weeks before the study (run-in period) allergic individuals recorded symptoms of conjunctivitis every day =
=
diary card (itching, photophobia, lacrimation, foreign-body sensation).2 No antiallergic drugs were allowed during the run-in. Conjunctival symptoms were more common in the pollensensitive patients than in the house-dust-mite-sensitive patients on a
.,.y..
B
E3
-
y
y ...........
Par jsensitive Dp sensitive subjects
Symptom scores on patients’ diary cards and sign scores and total cellular (cytology) scores reported by physicians. Par j = Pjudaica; Dp D pteronyssinus. =
(89% [185/207] vs 34% [67/193]). Furthermore, their clinical and
cytology scores were greater (figure). The controls showed neither clinical nor cytological reactions. All conjunctival scrapings of pollen-sensitive patients showed not only an inflammatory infiltrate (mainly neutrophils and eosinophils) but also several pollen grains (7-8 per field at 250 x focus); pollen granules frequently seemed to be ruptured along the outer envelope, thus releasing cytoplasmic contents. The greater severity of findings in pollen-sensitive subjects could be related to these granules in the conjunctiva. No pollen granules were found in conjunctival scrapings from the other patient group or from the controls. P judaica pollen grains are subspheroidal and are rapidly ruputed by osmotic shock (ie, contact with wet surfaces), releasing allergic contents through the germinal pore.2 Our findings fit very well with those of Suphioglu and colleagues. All these data suggest a combined mechanism whereby the conjunctiva of pollen-sensitive individuals selectively captures P judaica grains that trigger a specific-IgE-mediated response with inflammatory reaction, including the cellular infiltrate and mediator release.3 Moreover, histamine produces capillary leakage with albumin transudation, which could retain pollen grains, so prolonging allergen persistence and setting up a vicious circle with a clinically more severe pattern. A similar sequence could be hypothesised in pollen-associated asthma. Allergy and Clinical Immunology Service, Department of Internal Medicine and Eye Clinic, University of Genoa, 16132 Genoa, Italy, and Pathology Department, Alessandria Hospital
G. CIPRANDI S. BUSCAGLIA P. M. CERQUETI M. COSIMI G. W. CANONICA
Ciprandi G, Buscaglia S, Pesce GP, Marchesi E, Canonica GW. Protective effect of loratadine on conjunctival provocation test. Int Arch Allergy Clin Immunol (in press). 2. Solomon WM, Mathews KP. Aerobiology and inhalant allergens. In: Middleton E Jr, Reed CE, Ellis EF, Adkinson JF Jr, Yunginger JW, eds. Allergy: principles and practice, 3rd ed. St Louis: Mosby, 1988: 312. 3. Proud D, Sweet J, Stein P, et al. Inflammatory mediator release in conjunctival provocation of allergic subjects with allergen. J Allergy Clin Immunol 1990; 85: 1.
896-905.
Chlamydia pneumoniae infection and asthma SIR,-Dr Crane and colleagues (March 28, p 814) speculate that worldwide increases in asthma morbidity, mortality, and prevalence could be attributable to diagnostic transfer, changes in the delivery of health care, or increased diagnosis or self-reporting. I recent
would add another possible explanation that has not received the attention it deserves-increasing worldwide prevalence of Chlamydia pneumoniae infection. Preliminary epidemiological and clinical data support the suggestion that C pneumoniae infection may play a part in this increase in asthma. C pneunwniae infection has been associated with wheezing, asthmatic bronchitis, and adult-onset asthma in a clinical population.2 A patient from this study in whom asthma began in association with serologically confirmed acute C pneumoniae infection had a complete remission of symptoms after lengthy anti-chlamydial therapy. After a symptom-free interval of two
1174
years, this patient had renewed chronic wheezing in association with a serologically documented reinfection with C pneumoniae. In Finland, increasing prevalence of C pneumoniae infection since the 1970s3 correlates with striking increases in adult asthma 4 Since
C TRACHOMATIS IN FAMILIES OF SEVEN POSITIVE "ASTHMATIC" CHILDREN (A-G)
C pneumoniae is a recognised cause of bronchitis, we should also increase in acute bronchitis in adults that correlates with a rise in adult asthma between 1970 and 1981 in England and Wales.s There is also a temporal relation between the appearance of C pneumoniae infection6 and adult asthmain Denmark. I agree with Crane et al that appropriate use of bronchodilator medication is important to keep to a minimum the adverse effects on asthma. I would urge asthma researchers also to consider the possibility that C pneumoniae infection could be one of the underlying (and potentially treatable) causes of a disease whose management has so far been only palliative.
note an
Arcand Park Clinic, 3434 East Washington Ave, Madison WI 53704, USA
DAVID L. HAHN
1. Bone RC.
Chlamydial pneumonia and asthma: a potentially important relationship. JAMA 1991; 266: 265. 2. Hahn DL, Dodge R, Golubjatnikov R. Association of Chlamydia pneumomae (strain TWAR) infection with wheezing, asthmatic bronchitis and adult-onset asthma. JAMA 1991; 266: 225-30. 3. Puolakkainen M, Ukkonen P, Saikku P. The seroepidemiology of Chlamydiae in Finland over the period 1971 to 1987. Epidem Infect 1989; 102: 287-95. 4. Klaukka T, Peura S, Martikainen J. Why has the utilization of antiasthmatics increased in Finland? J Clin Epidermiol 1991; 44: 859-63. 5. Fleming DM, Crombie DL. Prevalence of asthma and hayfever in England and Wales. Br Med J 1987; 294: 279-83. 6. Grayston JT. TWAR. A newly discovered Chlamydia organism that causes acute respiratory tract infections. Infect Med 1988; 5: 215-48. 7. Pedersen P, Weeke ER. Epidemiology of asthma in Denmark. Chest 1987; 91: 107-14S.
Chlamydia trachomatis infection in children with wheezing simulating asthma SIR,-Ghlamydia trachomatis, according to WHO estimates is, after Trichomonas vaginalis, the most frequent sexually acquired pathogen in adults, carrying the possibility of contamination at birth of babies bom to infected mothers. It is difficult to establish how older children become infected with this organism, sexual abuse apart, but serological evidence of C trachomatis is found in an increasing proportion of the population with time. The rate varies not just with age but also with socioeconomic and environmental factors; in prepubertal age groups, rates of 26-7% and 47 2% have been reported.1,2 We have looked for C trachomatis infection in 20 wheezing children (13 boys, 7 girls; aged 6 months to 10 years, mean 32 months). They were negative on allergic evaluation and did not respond to bronchodilator agents. Pharyngeal and conjunctival swabs, for culture on McCoy cells and for a direct immunofluorescent test with monoclonal antibodies, were collected. In an attempt to trace the route of transmission we also examined the families of positive children. C trachomatis was identified by culture in 7 (35%) children in the pharynx, with concordance of results by both methods in only 1 case. In these 7 children, the organism was identified in the conjunctiva in 6; 4 of these had eye symptoms, present at the time of examination in 2. Treatment with erythromycin ethylsuccinate (50 mg/kg daily) for 2 weeks was successful in 6 of the 7 cases. In the other child, a further course of the same antibiotic eradicated the infection. C trachomatis was demonstrated by culture of at least one site in several parents of positive children (table). In one family, where the parents were both negative, we found on further inquiry that other relatives living in the same apartment were positive. Doxycycline 200 mg twice a day for 21 days was given to the adult relatives and the cousin was treated with erythromycin for 2 weeks. Control swabs after completion of this therapy were all negative. The asthmatic symptoms remitted in all 7 C trachomatis infected children, and the ocular symptoms also stopped. At 1-year follow-up these 7 children remained negative for C trachomatis on culture and had had no further asthma attacks. C pneumoniae strain TWAR can be excluded as the explanation in these 7 wheezing children because this agent grows only on HeLa
*Results for culture, immunofluorescence t- irrelevant or not done
(direct)
=
229 cells and
not on
the
McCoy
cells
we
used for
our
isolation
procedures. In these
children, C trachomatis infection could have arisen
through family contacts, the trigger being a primary infection in one adult.3 The findings in the family living in an overcrowded apartment suggest the possibility of C trachomatis spreading to children from adults directly by close daily contact with secretions (eg, saliva, tears) and/or hands or indirectly through fomites, toys, towels, and bedlinen, for example. Our data indicate that wheezing may be another clinical expression of C trachoma tis infection and that this organism should be sought as a routine in children who wheeze but have no demonstrable allergy and do not respond to the usual anti-asthmatic medications.
Supported by grant 9103613 from CNR P.F. FATMA. Institute of Paediatrics, La Sapienza University, and CNR Institute of Experimental Medicine, 00161 Rome, Italy
MARIA BAVASTRELLI MARIO MIDULLA DANIELA ROSSI MARCO SALZANO
1. Black SB, Grossman M, Cles L, Schachter J. Serologic evidence of infection in children. Pediatr 1981; 98: 65-67. J 2. San Joaquin VH, Rettig PJ, Newton JY, Marks MI. Prevalence of antibodies in children. Am J Dis Child 1982; 136: 425-27. 3. Medici A, Sollecito D, Rossi D, Midulla M. Family outbreak of trachomatis. Lancet 1988; ii: 682.
chlamydial chlamydial
Chlamydia
Reversal by ceftriaxone of dilated cardiomyopathy Borrelia burgdorferi infection SIR,-Dilated cardiomyopathy is a life-threatening disorder, which, when progressive, leads to chronic heart failure. It has been suggested that, in several cases, Borrelia burgdorferi could be associated with chronic myocarditis and dilated cardiomyopathy. Thus B
burgdorferi could be isolated and cultured from a myocardial biopsy specimen in a patient with dilated cardiomyopathy.1 However, data about B burgdorferi in dilated cardiomyopathy and its treatment are scant, especially with respect to reversibility of changes in myocardial functions We report a prospective study in which we examined specifically for B burgdorferi infection, serum for IgG and IgM (ELISA), and the history in 42 patients with dilated cardiomyopathy (mean left-ventricular ejection fraction [LVEF] 30% [SEM 12%] assessed by cardiac catheterisation). 9 (21 %) patients with a mean LVEF of 34% (2-2%) were seropositive for B burgdorferi, and 7 of those had a typical history of tick bite and erythema chronicum
